Abstract
The cutaneous immune response is important for the regulation of skin aging well as for the development of immune-mediated skin diseases. Aging of the human skin undergoes immunosenescence with immunological alterations and can be affected by environmental stressors and internal factors, thus leading to various epidermal barrier abnormalities. The dysfunctional epidermal barrier, immune dysregulation, and skin dysbiosis in the advanced age, together with the genetic factors, facilitate the late onset of atopic dermatitis (AD) in the elderly, whose cases have recently been on the rise. Controversial to the healthy aged skin, where overproduction of many cytokines is found, the levels of Th2/Th22 related cytokines inversely correlated with age in the skin of older AD patients. As opposed to an endogenously aged skin, the expression of the terminal differentiation markers significantly increases with age in AD. Despite the atenuated barrier disturbances in older AD patients, the aged skin carries an impairment associated with the aging process, which reflects the persistence of AD. The chronicity of AD in older patients might not directly affect skin aging but does not allow spontaneous remission. Thus, adult- and elderly subtypes of AD are considered as a lifelong disease.
Highlights
Aging is a genetically determined natural phenomenon that leads to the progressive deterioration in physiological integrity, functional capacity, and morphological features of the organism [1]
They accumulate in the papillary dermis of aged skin, where they are localized to macrophages and vasoactive intestinal peptide (VIP)
Immunological Changes in atopic dermatitis (AD) Development In AD, there exists a reciprocal relationship between the skin barrier dysfunction and the immune response, and both are necessary for the development of the disease
Summary
Aging is a genetically determined natural phenomenon that leads to the progressive deterioration in physiological integrity, functional capacity, and morphological features of the organism [1]. The main environmental stressors are ultraviolet radiation (UVR) [5,12,13], tobacco smoking [14,15], and other pollutants and toxins [16,17], as well as microbial insults. They contribute to premature skin aging with wrinkling formation and pigmentation affecting predominantly the exposed areas of the body (face, neck, head, and hands). Chronic sunlight exposure leads to superposition of the solar damage on the natural aging process resulting in chronic inflammation, impaired regenerative capacity, and carcinogenesis, associated with photoaging [18]. Skin in advanced age has insufficient perspiration and is susceptible to pervasive dryness and pruritus, infections, vascular complications (senile purpura, telangiectasia, etc.), and pigmentary changes (senile lentigines, etc.) [23]
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